But I feel you. I have myalgic pain since forever, I was bitten by a tick when I was a child ad got chronic myalgic pain afterwards that has been much better since taking rapamycin and just reducing this pain and reducing my skin seborrheic dermatitis is worth it. On the other hand it has messed a bit with my lipids and since they were always good enough (not perfect) but always in range it is in a way strange seeing the elevated status. And there is som much conflicting informations about lipids and lowering strategies and it is absolutely difficult to have a clear picture beyond reasonable doubt. I decided to nothing in terms of adding any lipid lowering medicines in the next 6 months (until I am taking rapamycin for a year).
I last took Rapamycyin (6mg) on 9th Sept (9/9). My LDL (UK units) was 3.51 on 6/9-uk (9/6-usa) and 3.14 on 12/9-uk (9/12-usa). I only have ApoB for the second test at 84mg/dL.
I use different labs because each lab has its own good and bad points. The prior dose of rapamycin was in July. Actually my glucose on 12/9 (9/12) was 4.99mmol/L (almost 90mg/dL) and HbA1c was 4.4787 (25.45 mmol/l prior week 27.1)
When I used the CGM it was possible to see an impact of Rapamycin, but I wonder if the frequency of usage of Rapamycin affects things like HbA1c and LDL-C/ApoB.
Although I used it relatively recently (only a few days before the test) it may be that my unusually low frequency of use of Rapamycin means that its effect on LDL-C and HbA1c is much lower as for most of the time it is not in my system at a threshold that has any real impact.
My view on atherosclerosis is that it is primarily caused by senescence in the epithelial cells which is exacerbated by lipids in some way.
I am not worrying about the fact that my LDL-C is wandering between 2 and 3 (the UK threshold for concern is 3 (mmol/L) partially because it wanders around and partially because I think I am handling senescence reasonably well and partially because ApoB is OK anyway.
A nice review of lipid management in Life Extension this month. They make some sound arguments for extreme lowering, but also that it’s not for everyone and not practical for everyone. That may be true if your goal is to live an average lifespan, but maybe aggressive intervention is necessary to get to a healthy 120. Or maybe many of us are genetically protected and will never have a cardiovascular event.
@rivasp12 Thanks for the insightful article. I agree that LDL should be lowered. However my experience with Rosuvastatin has been an utter failure. Do you think Ezetimibe and Bempedoic acid should be the next step? I really don’t think I can live with the myalgia from Rosuvastatin. Do you think a different statin may not have the same side effects? Thanks.
No I am taking a break from statins, figuring out if I should do a more like a Lustgarten approach too, partly because I am lazy about making new capsules. It didn’t really lower my apoB as I wanted probably because I already have low levels, but I don’t know for sure yet. Will def try them again or something else because of my APOE4 allele.
Taking citrus bergamot, as you so clearly stated, has been “an expensive failure” for me as well (tried for nine months with LDL moving from 172 to 164, and that could have been solely differences in what I ate the day before. It was “prescribed” by my doctor as a way to lower LDL My n=1 was a failure.
I am not sure why there is not more interest in lowering cholesterol and lipids with pantethine a natural over-the-counter supplement. I am not currently taking a statin. I have been taking ezetimibe and pantethine for cholesterol and lipid control. They are working better than the statin I was taking (Lipitor). Neither ezetimibe nor pantethine has any detectable side effects that I can tell.
“Pantethine, a derivative of vitamin B5, favorably alters total, LDL and non-HDL cholesterol in low to moderate cardiovascular risk subjects eligible for statin therapy: a triple-blinded placebo and diet-controlled investigation”
“After 16 weeks of treatment, significant reductions of total cholesterol, LDL-cholesterol and LDL-C/HDL-C ratio could be observed.”
“None of the patients complained of adverse reactions due to the treatment with pantethine.”
Two supplements that some people swear by are citrus bergamot and berberine. They perhaps are good supplements, but they have done nothing very amazing for me. They are on my list of supplements to drop when they run out.
I just looked up panethine. Maybe I’m seeing the wrong item, but for the doses your paper references (900mg per day) it’s very expensive (not “very” for a drug, but “very” for a vitamin) : I found 60 pills at 250mg for $40 — that’s 15 days at 1,000mg/day, or $960 per year?
Here is the one I use. I only use 600mg once per day along with ezetimibe 10mg twice per day, once in the morning and once in the evening.
NOW Supplements, Pantethine (Coenzyme A Precursor) 600 mg, Double Strength, Cardiovascular Health*, 60 Softgels
On this study, Pantethine at 600 mg/day resulted in 11% decrease in LDL-c for patients (avg age 50-ish) with LDL above 160. I’m not sure this was statistically significant, but this is roughly what the papers on citrus bergamot described as well. 11% is decent, but isn’t gonna get me from 164 to 100. I think I may need more firepower.
I’ve always tended towards high cholesterol, and only ONE thing has made a meaningful dent: thyroid T3
Not actively promoting this - it was a byproduct of an irresponsible experiment taking T3 (long story). But I think it’s worth thinking about, and I may try it again for that purpose.
It makes sense: T3 is used to convert cholesterol to important downstream products, effectively increasing demand on available cholesterol. Statins instead reduce cholesterol “supply”.
In my experience, I was taking relatively high doses of T3 throughout the day. After a couple months of this I had my usual blood test - and all my cholesterol numbers were significantly below reference. Frighteningly so, actually, and I stopped the T3.
I did read btw that thyroid historically was used for cholesterol control, but was dropped in favor of more modern (and possibly more profitable) drugs. I don’t knew if this is true however.
Anyway, I may experiment again with thyroid, probably T4 (Levothyroxine) which has a much longer half life, and this time be more cautious about what it actually does.
My daughter was prescribed levothyroxine along with a low dose of rosuvastatin and it dramatically lowered her cholesterol and lipids. Unfortunately, they were prescribed together so it is hard to tell which one or both caused the decrease. Maybe they work synergistically. She has had no side effects from taking the combo.
Testing biomarkers, tracking food, nutrition, supplements, correlations with biomarkers. Means I need to build data of a baseline first before starting any med.
A relaxed approach to lipids doesn’t make sense to me.
I’ve tried multiple statins and they make me feel 100 years old. I can’t help but wonder what they’re doing to make me feel like that. Probably very individual.
I’d try one at a time at low dosing and increase as tolerated. The problem is that it may take multiple meds to get extreme lowering.
This is very interesting. I’ve had my T3/TSH tested before and am not hypothyroid (although no hyper either). I see papers that show lowering LDL is effective in hypothyroid patients, and not so for hyperthyroid patients. I don’t see anything on how it can help/not help people who are neither.
It also got me thinking if the “range” for thyroid function is lowered by age? Meaning if I had the thyroid of a 25 year old would my “normal” levels be higher than what I have been told is normal for a 50-ish guy? Aren’t we all tending toward hypothyroidism anyway (isn’t that what Brian Fahe is testing?) so if I supplemented T3 would it bring me back to younger thyroid function while lowering my LDL in the process?